Ectopic expression of B7-1 (CD80) on T lymphocytes in autoimmune lpr and gld mice
Defective Fas-mediated apoptosis in mice, caused by the gld mutation in the fas ligand gene, results in the development of lupus-like autoantibodies and severe lymphoproliferation. We previously demonstrated ectopic expression of the costimulatory molecule B7-1 (CD80) on T lymphocytes in B6/gld mice...
Veröffentlicht in: | Clinical immunology (Orlando, Fla.). - 1999. - 91(1999), 3 vom: 01. Juni, Seite 302-9 |
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Format: | Aufsatz |
Sprache: | English |
Veröffentlicht: |
1999
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Zugriff auf das übergeordnete Werk: | Clinical immunology (Orlando, Fla.) |
Schlagworte: | Journal Article Research Support, U.S. Gov't, P.H.S. Antigens, CD Antigens, Differentiation B7-1 Antigen CD28 Antigens CTLA-4 Antigen Ctla4 protein, mouse Fas Ligand Protein Fasl protein, mouse mehr... |
Zusammenfassung: | Defective Fas-mediated apoptosis in mice, caused by the gld mutation in the fas ligand gene, results in the development of lupus-like autoantibodies and severe lymphoproliferation. We previously demonstrated ectopic expression of the costimulatory molecule B7-1 (CD80) on T lymphocytes in B6/gld mice. This report extends these observations by demonstrating similar results in B6/lpr mice, which possess a mutation in the gene encoding Fas. Additionally, we demonstrate that this phenomenon is age-dependent and occurs on multiple subsets of B6/gld T lymphocytes. B7-1 upregulation is observed on T cells from both conventionally housed and specific-pathogen-free B6/gld mice, suggesting that this is not a consequence of infection by pathogen. T cells from lpr and gld mice show increased binding of CTLA4-Ig fusion protein, suggesting that the upregulated B7-1 is functional. CD28, a receptor for B7-1 which activates T cells, is upregulated in B6/lpr and B6/gld mice, while CTLA4, a negative regulator of T cells which binds B7-1, is not. Our results suggest that ectopic expression of B7-1 on T cells of lpr and gld mice may be playing a role in exacerbation of lymphoproliferation and/or autoimmunity |
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Beschreibung: | Date Completed 25.06.1999 Date Revised 16.11.2017 published: Print Citation Status MEDLINE |
ISSN: | 1521-7035 |